PBL case Brief

Mary 23rd year old women brought in by ambulance from a music festival presenting with
drowsiness, slurred speech, dyspnea and has vomited three time on a background of poorly
controlled Type 1 diabetes. She had missed her last two insulin dosage and had some food intake
during the day. DKA was suspected and was later confirmed with glucometer and urinalysis
showing a hyperglycaemia and presence of ketones. Her blood results showed metabolic acidosis
with ph of 7.12 and bicarbonate at 15. She had some electrolyte and dehydration but was not
hypokalaemic. Therefore, she was immediate managed with 2000mls of 0.9% saline IV, quick
acting insulin infusion of 5 units per hour. When Mary was stable maintenance IV fluid with
potassium was provided at 100mls per hour.
Precipitating factors include atypical pneumonia (confirmed by CXR) with right base crackles and
a candida vaginal infection confirmed by swab. IV azithromycin and fluconazole treatment was
provided.
Diabetic history
Regarding Marys diabetic history she was diagnosed with Type 1 DM at 19 presenting with
increased urinary frequency. Her initial and current treatment consist of twice daily insulin.
Although seen by a dietician, there is poor dietary compliance due to concerns with friends and
colleagues finding out her diagnosis and weight gain.
She has had multiple hypoglycaemia attacks with one requiring IV glucose from paramedics but
was not admitted into hospital. Due to hypoglycaemic attack she had stopped insulin and had
symptoms including polyuria,polydipsia, blurred vision and vaginal irritation. Her insulin dose was
lowered.
She admits to poor insulin use and often forgets to test her BGL.
Social history
Mary has not told anyone of her diabetes except for her boyfriend. She is a drama teacher and
fears impact of diabetes on her job and her ability to maintain her drivers license.
She is currently on OCP and hopes to have children in the future.
Summary
In summary, 23 year old female with Type 1 diabetes presenting with DKA due to missed insulin
dose, poor diabetic control and possibly precipitated by atypical pneumonia and vaginal candidal
infection. She was stablised with insulin and fluids and treated for the infections. Her medication
compliances, diet and social support will need to be addressed. Education on this as well as
diabetes control for pregnancy planning should be discussed.

Mechanism of Type 1
-

Autoimune beta cell deustrction (mostly)

o Some have clinical phenotype of type 1 but lack immunologic markers of
autoimmune process. Development of insulin deficiency by unknown process and are
ketosis prone (African American or Asian heritage)

This graph shows the function of beta cell mass

70-80% before diabetic features, the residual functional beta cells cannot maintain glucose
tolerance.
There is a honeymoon phase post diagnosis which is the phase in which the patient may not
require that much insulin. This goes away but some patients can be seen with C peptide
production = small amounts of insulin production.

Genetics
HLA complex Chromosome 6 involing MHC. Most indivudlas have HLA DR3 or DR4

However the risk of low for first degree relatives

Pathogenesis of DM1
-

Insulitis with T lymphocyte infiltration

Autoantibodies do not generally react with cell surface of islet cells
THUS the islet dustruction is mostly mediate by T lymphocytes rather than islet
autoantibodies.
B cells are particularly suspectible to toxic effects of TNFa, IFNy and Il1

DKA pathophysiology
-

Insulin deficiency with counterregulatory hormone excess (glucagon, catecholamine,

cortisol, growth hormone)
Insulin:glucagon ratio decreases resulting in gluconeogenesis, glycogenolysis and ketone
body formation
Glucagon decreases activity of pyruvate kinase
Insulin deficiency increases phosphoenolpyruvate carboxykinase = glucose synthesis and
less glycolysis.

Ketosis
-

Marked increase in free fatty acid release from adipocytes

This is due to reduced insulin, increased catecholone and growth hormone
Increase lipolysis and release free fatty acid

When can DKA occur?

-

Increased insulin requirement when there is concurrent illness

Complete or inadequate insulin

DKA diagnosis
-

Hyperglycaemia, ketosis and metabolic acidosis (increased anion gap)

However BGLl can be minimally elevated
Serum bicarb is <10 and pH ranges 6.8 to 7.3 depending on the severity
Potassium can be mildly elevated secondary to acidosis
Sodium, chloride, phosphorus and magnesium and reduced in DKA
Increased BUN and creatinine serum = volume depletion
Increased lipid profile (risk of pancreatitis)

Treatment of DKA
-

IV fluid replacement and insulin therapy (haemodynamic stability and adequate urine
output)
o Use of short acting insulin
o Mild can use SC but IV insulin used for those with acidosis and metabolic unstability
If vomiting = nasogastric tube to prevent aspiration